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Biomedical subjects

G K Yim

Publications and source records attributed to G K Yim.

At least 55 records · Page 3Linked to original sources
PubMed1985

Opioid modulation of feeding behavior following repeated exposure to forced swimming exercise in male rats.

Patterns of normal and stimulated food intake (FI) as well as its possible endogenous opioid (EO) modulation were investigated in male rats given regular swimming exercise (trained; TR) and compared with nonexercised sedentary (SED) controls. Rats in the TR group had lower body weights as well as reduced 24 hr FI due to lower nocturnal FI. TR rats also ate less food in response to injections of 2-deoxy-D-glucose (2-DG) but not insulin (INS) when injections were given during the first 4-5 weeks of training. However, this difference between TR and SED rats in the 2-DG induced feeding was not demonstrable after 10 or more weeks of training. Plasma concentrations of immunoreactive B-endorphin (IR-B-ep) were elevated, as expected, in TR rats (10-12 weeks) during nocturnal sampling whereas the nocturnal increase of IR-B-ep was absent in SED controls. However, these SED rats did increase daytime IR-B-ep in response to 2-DG and acute exercise, albeit somewhat less in magnitude when compared to TR rats. Injection of naltrexone (NTX) decreased feeding in TR rats (10-12 weeks) but not in contemporary SED controls. In summary, exercise training modified feeding behavior, and at 4 weeks of training, TR rats ate less in response to opioid-related feeding stimulus of 2-DG, but responded similarly to insulin (relatively opioid independent) treatment. At later stages of training this difference between TR and SED rats disappeared. Moreover, SED rats had atypical profiles of IR-B-ep and reduced hypophagic responses to NTX suggesting that TR rats might have greater EO modulation of feeding at this stage.

Animals↗
PubMed1984

Therapeutic reduction of ongoing carrageenin-induced inflammation by lipoxygenase, but not cyclooxygenase inhibitors.

A variety of steroidal and nonsteroidal antiinflammatory agents (NSAs) were compared for their effectiveness against a developing acute inflammatory reaction. Only BW 755C [3-amino-1-(m-trifluoromethyl)-phenyl-2-pyrazole] was immediately effective when administered 2 h after carrageenin, as the 3-h swelling was significantly reduced. Dexamethasone, a steroidal antiinflammatory agent, produced a delayed reduction. When administered at 2 h postcarrageenin, there was no effect at 3 h; but at 6 h, dexamethasone significantly reduced the swelling. In contrast, neither of the classic NSAs, aspirin or indomethacin, were effective when administered after the carrageenin. The results demonstrating a postcarrageenin effectiveness by BW 755C and dexamethasone are discussed as a possible reflection of an action on the lipoxygenase pathways of the arachidonic cascade that is not shared by the classic NSA.

4,5-Dihydro-1-(3-(trifluoromethyl)phenyl)-1H-pyraz↗
PubMed1984

Differential inhibition by propranolol of feeding induced in rats by various stimuli.

Opiate receptor blockade, or forced imbibition of 2% NaCl to deplete pituitary dynorphin decreases 2-deoxy-D-glucose (2-DG), but not insulin-induced hyperphagia, indicating a possible role for dynorphin in the eating associated with endogenous opiates. Beta-adrenergic receptor blockade decreases vasopressin release induced by 2-DG but not by insulin. Because vasopressin and dynorphin are sometimes co-localized, it was hypothesized that naloxone-sensitive feeding might be selectively inhibited by beta-adrenergic blockade with propranolol. Propranolol in doses as low as 2.5 mg/kg inhibited 4 hr feeding induced by 2-DG (400 mg/kg). Propranolol did not significantly affect feeding induced by ketocyclazocine administration (3.0 mg/kg) or by 24 hr food deprivation. Feeding stimulated by insulin (10 U/kg) was significantly inhibited by propranolol (2.5 mg/kg) only when the propranolol was reinjected during the period 2 hr after insulin injection, when the induced feeding was greatest. In summary, propranolol inhibited opiate-related (2-DG) as well as opiate-independent (insulin) hyperphagias. It also failed to inhibit food intake resulting from the opiate related stimulus of 24 hr food deprivation. Therefore, naloxone sensitive hyperphagias were not specifically inhibited by beta-adrenergic blockade, indicating that vasopressin-associated dynorphin is not involved in opiate related feeding.

Animals↗
PubMed1984

Stress, endogenous opioids and salt intake.

The effect of stress on NaCl intake was examined in mice given a choice of water and 1.5% NaCl to drink. Immobilization of mice for 15-min and 24-h food deprivation resulted in a 2.5- and 5-fold increases in NaCl intake, respectively, without affecting water intake. Naloxone treatment (0.01, 0.1 and 1.0 mg/kg) produced a dose-dependent decrease in the stress-induced NaCl intake, as did captopril treatment (5, 10 and 50 mg/kg). Intraventricular injection of angiotensin II in mice resulted in an increase in 1.5% NaCl intake, which was blocked by naloxone. Morphine (10 mg/kg) increased the preference of mice for a normally aversive 3.0% NaCl solution, but not for preferred, less concentrated, solutions of NaCl. The results suggest that both endogenous opioids and angiotensin II contribute to stress-induced NaCl intake, and that endogenous opioids may also mediate the increase in NaCl intake, observed with angiotensin II.

Angiotensin II↗
PubMed1984

Opioids, feeding, and anorexias.

This review summarizes recent work that focuses on the role of endogenous opioids (EOs) and opiate receptors in the control of food intake. Although the anorexic effect of opiate antagonists are now well accepted, the exact EO, site(s), and mechanism(s) of action remain to be established. However, accumulating evidence suggests that dynorphin, an endogenous ligand for kappa-type opiate receptors, is an important regulator (stimulant) of appetite. The roles of other EOs, such as beta-endorphin, are less clear. EOs appear to be involved in maintaining normal feeding behavior and are likely responsible for the overconsumption of fat in genetically obese and stressed subjects. Opiate antagonists block overconsumption of palatable foods, thus offering a promising approach to weight reduction for some overweight individuals. Anorexias may follow from a deficiency of kappa-type opioid activity, and surprisingly, can also result from excess opioid activity. Indeed, opiate antagonists of the mu type (naloxone) can enhance eating and weight gain in certain anorexic conditions. Therefore, it appears that excess opioid agonist activity may result in hyperphagia or anorexia (depending on the opiate receptor type). Finally, opiate antagonists may help normalize both types of pathological feeding states.

Animals↗
PubMed1984

Effect of acute and repeated chlordimeform treatment on rat hepatic microsomal drug metabolizing enzymes.

The effect of chlordimeform treatment on the hepatic microsomal drug metabolizing enzymes was examined in male and female rats following either acute or repeated treatment. After acute administration of chlordimeform (100 mg/kg, ip one hr prior to sacrifice) differential effects were observed in various parameters of the hepatic microsomal mixed function oxidase system with significant decreases in ethylmorphine metabolism, cytochrome P-450 content, NADPH cytochrome c reductase, and in the spectral binding of hexobarbital and aniline while no changes were found in the metabolism of aniline or p-nitroanisole. Durations of zoxazolamine-induced paralysis and pentobarbital-induced hypnosis were increased significantly after acute chlordimeform administration. Following repeated administration of chlordimeform (75 mg/kg ip for four days) to adult male rats, a decrease was observed in zoxazolamine-induced paralysis time while pentobarbital-induced hypnosis was not altered. Metabolism studies using isolated hepatic microsomal fractions showed a decrease rate of biotransformation of ethylmorphine and aniline while the activity of p-nitroanisole O-demethylase was not changed. No differences were found in cytochrome P-450 levels whereas microsomal spectral binding of hexobarbital was reduced while that of aniline was not affected. Following acute or repeated administration of chlordimeform to adult female rats, decreases in the hepatic microsomal metabolism of aniline, but not ethylmorphine or p-nitroanisole, were observed. Addition of chlordimeform to microsomal suspensions yielded a Type I spectral binding curve.

Amidines↗
PubMed1984

Central and peripheral anti-inflammatory actions by clonidine and a structurally related imidazoline analog.

Systemic (i.p. and p.o.) administration of clonidine significantly reduced the acute inflammatory swelling of the rat paw produced by carrageenin, histamine and serotonin. Clonidine did not reduce carrageenin swelling when given i.c.v. Intraperitoneal administration of a structural analog of clonidine, 2-(2-methyl-4- chlorophenylamine ) -2-imidazoline (CDMI), was only effective against carrageenin swelling. CDMI was 10 times more effective when given centrally (i.c.v.) than when given systemically (i.p. or p.o.). The slopes of the individual dose-response curves were not significantly different which suggested a common mechanism of action. However, although adrenalectomy did not reduce the anti-inflammatory activity of i.p. CDMI, i.c.v. CDMI was ineffective in adrenalectomized rats. These results indicate that imidazolines represent a unique class of anti-inflammatory agents with actions mediated both peripherally and centrally.

Adrenalectomy↗
PubMed1983

In vitro and in vivo evaluation of cis-methyl-phencyclidine (CIS-MPCP) as a potential antagonist of phencyclidine (PCP).

In four preparations/tests (isolated nerve, ventricular strip, rotarod, and mouse acute lethality), cis-N-phenyl-4-methyl-cyclohexyl piperidine (cis-MPCP) was consistently less active than PCP and trans-MPCP. As expected, cis-MPCP, at 10(-4)M, which did not depress the action potential evoked on frog sciatic nerves, reduced by half both the nerve block and prolongation of relative refractory period caused by PCP. However, cis-MPCP at 10(-6)M, which by itself had little effect, failed to reduce the positive inotropic effect of PCP on the field-stimulated rat ventricular strip. Cis-MPCP also failed to decrease the ataxic effect of 6 mg/kg PCP (ED80) in the mouse rotarod test. Finally, at a dose that was neither ataxic nor lethal to mice (20 mg/kg), cis-MPCP failed to reduce the 24-hour LD50 of PCP. These data suggest that the actions of PCP are mediated through a multiple receptor system.

Action Potentials↗
PubMed1983

Block by phencyclidine of acetylcholine and barium induced adrenal catecholamine secretion.

Activation of the sympathetic system by phencyclidine (PCP) should result in catecholamine release from the adrenals. However, adrenalectomy does not reduce PCP-induced hypertension. In an attempt to rectify this inconsistency, the direct effects of PCP on the bovine adrenal medulla were examined. At (3 X 10(-6) M), PCP reduced the acetylcholine-(ACh)-induced catecholamine release by 50%. Surprisingly, barium-induced secretion of catecholamines was also reduced by PCP. ACh-induced catecholamine release was not altered by 10(-3)M 4-aminopyridine (4 AP), the potassium channel blocker. Thus, calcium antagonist actions of PCP and consequent block of catecholamine secretion from adrenal medulla may explain the lack of effect of adrenalectomy on PCP-induced hypertension. Possible contributions of calcium and/or potassium channel blockade to other manifestations of PCP overdosage are discussed.

4-Aminopyridine↗
PubMed1983

Increased central serotonergic activity associated with nocturnal anorexia induced by Walker 256 carcinoma.

The role of brain serotonin levels in Walker 256 tumor induced anorexia was investigated. Total and free plasma tryptophan, regional brain serotonin and 5-hydroxyindoleacetic acid were determined at night, and their relationship to nocturnal anorexia assessed by linear regression analysis. No significant difference in tryptophan, serotonin, or 5-hydroxyindoleacetic acid levels was detected between pair fed and tumor bearing rats exhibiting a 20% reduction of nighttime food intake. Tumor bearing rats with a 40% reduction in food intake had higher nighttime plasma free tryptophan and regional 5-hydroxyindoleacetic acid levels than their pair fed malnourished controls. These results indicate that increased plasma free tryptophan and elevated serotonin metabolism may not be the initial dysfunction responsible for nocturnal anorexia. However, it may contribute to the decreasing nocturnal food intake in severely anorexic tumor rats.

Animals↗
PubMed1983

Stimulation of food intake following opiate agonists in rats but not hamsters.

The proposed mu and kappa opiate receptor agonists morphine and ketocyclazocine, as well as meperidine, were compared for their ability to stimulate feeding and drinking by male rats and hamsters that were not deprived of food or water. Morphine (8.0 mg/kg) and ketocyclazocine (0.5-4.0 mg/kg), but not meperidine (0.5-64.0 mg/kg), increased 3-h food intake by rats. By 6 h the hyperphagic responses were less pronounced. However, 6-h water intake was increased by all three agonists. In contrast to rats, hamsters failed to increased food or water intake over an 8-h period following morphine (6.25-800 mg/kg), ketocyclazocine (0.25-16.0 mg/kg), or meperidine (1.0-128 mg/kg) administration. Thus, kappa or mu opiate receptors may mediate the observed hyperphagic effect of opiate agonists on rat food intake. In addition, these results are consistent with our earlier suggestion that hamsters lack an opiate-sensitive feeding system.

Animals↗
PubMed1983

Opioid modulation of appetite.

The discovery of opiate receptors and endogenous opioid peptides within the central nervous system has resulted in a number of speculations concerning the physiological significance of these peptides. In the present article, we review the evidence suggesting a primary role for some of the opioid peptides as regulators of ingestive behavior. In particular, we elaborate a hypothesis in which we suggest that in some species opioid peptides may play a role as a tonic inducer of ingestive behaviors, held in check by a variety of neuropeptides and monoamines. This review explores in detail the role of the opioid peptides as major mediators of the reward system and as a link between reward and feeding behaviors. Finally, a teleological role for opioid peptides in species preservation, which may explain the discrepancies in the role of the opioid peptides in feeding behavior in different species is proposed. It is suggested that the feeding profile of the animal provides important clues as to whether or not the animal has an opiate-sensitive feeding system. We stress that interactions with ingested nutrients and the milieu interieur provide an important means by which animals modulate the opiate-entrained feeding drives.

Animals↗
PubMed1983

Effect of acute and repeated chlordimeform treatment on rat hepatic microsomal drug metabolizing enzymes.

The effect of chlordimeform (CDM) treatment on the hepatic microsomal drug metabolizing enzymes was examined in male and female rats following either acute or repeated treatment. After acute administration of chlordimeform (100 mg/kg, i.p., 1 hour before killing) differential effects were observed in various parameters of the hepatic microsomal mixed function oxidase system with significant decreases in ethylmorphine metabolism, cytochrome P-450 content, NADPH cytochrome c reductase, and in the spectral binding of hexobarbital and aniline while no changes were found in the metabolism of aniline or p-nitroanisole. Durations of zoxazolamine-induced paralysis and pentobarbital-induced hypnosis were increased significantly after acute CDM administration. Following repeated administration of CDM (75 mg/kg, i.p., for 4 days) to adult male rats, a decrease was observed in zoxazolamine-induced paralysis time while pentobarbital-induced hypnosis was not altered. Metabolism studies using isolated hepatic microsomal fractions showed a decreased rate of biotransformation of ethylmorphine and aniline while the activity of p-nitroanisole O-demethylase was not changed. No differences were found in cytochrome P-450 levels whereas microsomal spectral binding of hexobarbital was reduced while that of aniline was not affected. Following acute or repeated administration of CDM to adult female rats, decreases in the hepatic microsomal metabolism of aniline, but not ethylmorphine or p-nitroanisole, were observed. Addition of CDM to microsomal suspensions yielded a Type I binding curve.

Amidines↗
PubMed1983

Local anesthetic activity and disopyramide toxicity.

In the isolated frog sciatic nerve preparation, IC50 concentrations for nerve block were 0.34 +/- 0.9 mM for lidocaine (LIDO), 0.62 +/- 0.11 mM for procaine, 11.9 +/- 6.1 mM for disopyramide (DIP), and 52.8 +/- 24 mM for MIP (the mono-demethylated metabolite of DIP). In contrast to the LIDO block, DIP-induced nerve block was irreversible. DIP-induced depression of the electrically stimulated rat ventricular strip was completely reversed by washing the drug-free Tyrode's solution. In mice receiving 250 mg/kg DIP, neither convulsions nor death could be prevented by diazepam or other anticonvulsants. These results suggest that DIP has a very weak local anesthetic action which does not contribute significantly to disopyramide toxicity.

Action Potentials↗
PubMed1983

Therapeutic and adjunctive applications of an imidazoline anti-inflammatory agent.

A unique combination of anti-inflammatory and antiulcerogenic activities is described for 2-(2 methyl-4-chlorophenylamino)-2-imidazoline (CDMI). CDMI administered i.p. produced a dose-related decrease in aspirin-induced ulcers which persisted even in the presence of exogenously added HCI. The carrageenin-edema reducing activities of i.p. CDMI and p.o. aspirin were additive. When oral CDMI was combined with oral aspirin or oral indomethacin, the combinations also resulted in additive anti-inflammatory activities (80 and 94% vs. 52% for CDMI, 62% for aspirin and 71% for indomethacin alone). Moreover, gastric ulcerogenicity was reduced by 92% when either aspirin or indomethacin was combined with CDMI. These results indicate that CDMI and related compounds deserve further study as adjuncts to increase the margin of safety of currently used nonsteroidal anti-inflammatory agents. CDMI was also tested against a developing acute inflammatory reaction. When administered at 2 hr post carrageenin, CDMI was as effective as when it was administered 30 min before the carrageenin. These results are discussed as a possible reflection of an action on the lipoxygenase pathways of the arachidonic acid cascade that is not shared by the classical nonsteroidal anti-inflammatory agents.

Animals↗
PubMed1982

Drinking, but not feeding, is opiate-sensitive in hamsters.

The long-lasting opiate antagonist, naltrexone (NTX), was examined for its effects on various types of consummatory behavior in male golden hamsters and rats. Rat, but not hamster, 24 hr food and water intakes were significantly decreased by four daily NTX (10.0 mg/kg) injections. Hamsters displayed a minimal night to day feeding ratio compared to rats. Hamsters increased food intake following insulin (50 U/kg) administration, but not after 24 hr food deprivation (FD) or 2-deoxy-D-glucose (2-DG; 800 mg/kg) injections. NTX (1.0 and 10 mg/kg) had no effect on feeding, but markedly attenuated hamster drinking induced by 48 hr water deprivation or hypertonic saline injection. Dexamethasone (DEX), a glucocorticoid which depletes pituitary beta-endorphin and produces anorexia in rats, had no effect on daily hamster intake. Since the normal feeding profile of the hamster is similar to that of naloxone and DEX-treated rats, hamsters appear to lack an opiate-sensitive feeding system. In contrast, stimulated drinking behavior of hamsters operates through an opiate-sensitive mechanism. Thus, there are marked species differences concerning the involvement of endogenous opioids in consummatory behavior.

Animals↗
PubMed1982

Reduction by atropine of phencyclidine hypertension and apneusis.

The aim of this study was to assess the possible role of a central cholinergic component phencyclidine (PCP)-induced hypertension. Sprague-Dawley rats, lightly anesthetized with urethane, exhibited a dose related pressor response following 0.1-1.0 mg/kg PCP i.v. After i.v. atropine pretreatment, the PCP dose-response curve was shifted to the right, and the magnitude of the pressor responses was reduced by about 50%. In addition, atropine reduced the incidence of apneusis, but had no effect on the bradycardia that accompanied the pressor responses. Methylatropine (i.v.) did not reduce the PCP pressor responses, nor did it prevent the apneusis induced by PCP. These results suggest that in addition to its direct pressor effects the activation of central cholinergic systems contribute significantly to the cardiovascular and respiratory toxicity induced by PCP.

Animals↗